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ND630 controls ACACA and lipid reprogramming in prostate cancer by regulating the expression of circKIF18B_003

Yu-Peng Wu1,2, Wen-Cai Zheng1,2, Qi Huang1,2

  • 1Department of Urology, Urology Research Institute, The First Affiliated Hospital, Fujian Medical University, 20 Chazhong Road, Fuzhou, 350005, China.

Journal of Translational Medicine
|December 4, 2023
PubMed
Abstract

Insights

The drug ND630 regulates lipid metabolism and ACACA expression in prostate cancer by targeting circKIF18B_003. This study reveals circKIF18B_003 as a potential therapeutic target for prostate cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • ND630 is a novel molecule targeting ACACA and lipid metabolism, but its role in prostate cancer is unknown.
  • KIF18B is an oncogene crucial for prostate cancer progression, with its derived circRNA, circKIF18B_003, overexpressed in tumors.
  • This study investigates ND630's effect on prostate cancer via circKIF18B_003 regulation of ACACA and lipid reprogramming.

Purpose of the Study:

  • To determine if ND630 controls ACACA and lipid reprogramming in prostate cancer.
  • To investigate the role of circKIF18B_003 in prostate cancer progression.
  • To elucidate the regulatory mechanism of ND630 on circKIF18B_003.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR) for circKIF18B_003 expression analysis.
  • Cellular assays (CCK-8, colony formation, wound healing, Transwell) and xenograft models to assess circKIF18B_003 function.
  • RNA immunoprecipitation (RIP), RNA pull down, and luciferase reporter assays to explore molecular mechanisms, including circKIF18B_003 sponging of miR-370-3p.

Main Results:

  • circKIF18B_003 overexpression in prostate cancer tissues correlates with poor patient survival.
  • Upregulation of circKIF18B_003 enhances prostate cancer cell proliferation, migration, and invasion.
  • circKIF18B_003 acts as a sponge for miR-370-3p, increasing ACACA expression and promoting malignant phenotypes; this effect is reversed by ACACA downregulation.
  • ND630 combined with docetaxel significantly reduced tumor growth, indicating a role in lipid metabolism regulation.

Conclusions:

  • ND630 regulates ACACA and lipid reprogramming in prostate cancer by modulating circKIF18B_003 expression.
  • ND630 and circKIF18B_003 represent a promising novel therapeutic target for prostate cancer.
Keywords:
ACACACircRNAsND630Prostate cancer

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